Derm Final 2

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Describe the pathogenesis of atopic dermatitis.: Atopic dermatitis is â€œstrange diseaseâ€ and is a familial predisposition to the development of IgE antibodies and clinical allergy to environmental antigens
Describe the lesions and distribution pattern of atopic dermatitis: Lesions: -Erythema -Alopecia -Papules -Excoriations -Hypepigmentation -Lichenification Distribution: -Muzzle -Periocular -Axillae -Feet -Flexor surfaces of elbows and tarsus -Extensor surface of carpus -Lesions may become generalized in chronic cases
What are the advantages and disadvantages of RAST?: Advantages -Very specific Disadvantages -Poor reproducibility -Poor specificity for IgE -Many false positives -Great seasonal variability
What are the advantages and disadvantages of IDST?: Advantages -Gold standard for determining allergens -Shows whether or not an allergen is capable of producing skin lesions in the tested patient -Immediate results Disadvantages -Owners refuse clipping of fur -If skin does not respond to the histamine, it wonâ€™t respond to injected allergens -No access to the test
How do you interpret a negative IDST?: -Patient not allergic to reaction -SQ injection given -Insufficient antigen -Concurrent drugs blocked the skin test (this is why they must be off drugs before testing) -Prolonged allergy (exhaustion of IgE levels)
How do you interpret a positive IDST?: -Patient allergic to antige -Patient allergic to the cross reacting antigen -Irritants -Bacterial or fungal contamination -Antigen contains histamine -Too large volume injected
What are the advantages and disadvantages of using corticosteroids for the treatment of atopic dermatitis?: Advantages -Very effective at decreasing skin inflammation and itching Disadvantages -Many side effects (PUPD, panting, weight gain, increased risk of infection, ect.) -Use only if other therapies are not feasible
What are the advantages and disadvantages of using cyclosporine for the treatment of atopic dermatitis?: Advantages -Effective in severe allergy cases for decreasing skin inflammation and itching -Suppresses T cells and decreases IgE production -Decreases production of cytokine Disadvantages -Side effects (GI, renal, hepatic, bone marrow) -Costly
What are the advantages and disadvantages of using hyposensitization (immunotherapy) for the treatment of atopic dermatitis?: Advantages -Increases T suppressor cell activity, w/ gradual decrease in IgE -Blocks antibodies -Decreases number of mast cells and/or decreases histamine release from mast cells Disadvantages -May req. 9 months or longer to obtain maximal effectiveness -25-50% chance of not working or needed additional treatment
Discuss client education of the treatment of atopic dermatitis.: -Must communicate that the animal is a walking dust mite and they must be bathed frequently -Also, if animal is allergic to material in house or what owner wears, significant changes must be made -Owner must be committed to working w/ the disease or the animal will suffer for their entire life
Describe the MOA of glucocorticoids in treatment of allergy.: -Glucocorticoids block Cox 1 and 2 as well as phospholipase A (which is needed to make Prostaglandins)
Describe the benefits of antihistamines in cats and dogs: -Antihistamines are a good preventative drug, just not great for treatment -Block H1 and H2 receptors -Stabilize mast cells -Few side effects
Describe the physiological basis of alternate day steroid administration.: -Alternate day therapy is an attempt to control the animals atopy while giving them less drug. This will decrease the potential for side effects and resistance.
Are lamb and rice nonallergenic?: -NO- lamb and rice are not non-allergenic (many animals are, in fact, allergic to lamb)
Why are lamb and rice chosen for some hypoallergenic diet trials?: -Lamb and rice are chosen however for some hypoallergenic diets b/c lamb is a novel protein and if the animal has never tried lamb it might be worth a try. Rice is added in as the carbohydrate source
Devise a restrictive diet trial for a cat or dog for which you have been presented with a list of its past diet.: HOME COOKED DIETS -Choose a protein source that the animal has never been exposed to (lamb, fish, venison, rabbit, tofu, pinto beans) -Choose a carbohydrate source (brown rice, white rice, potatoe, green peas) -Mix the two as a 1 part protein : 3-4 part carbo STORE DIETS -Again look for a protein source the animal hasn't tried (Hill D/D, Z/D or Purina HA)
What are the DDX of a cat w/ pruritis on its head and neck.: -Food allergy -Ear mites -Notoedres -Flea allergy dermatitis
How can you differentiate allergic contact dermatitis from an irritant contact dermatitis?: Allergic Contact dermatitis: -An inflammatory skin disease caused by a delayed (cell-mediated) response to an antigen or hapten. Requires repeated or continuous exposure to the substance Irritant Contact Dermatitis: -An inflammatory skin disease which occurs within minutes of contact w/ irritating substance
Outline measures that can be used to minimize an animals exposure to housedust mites.: -Remove carpets, blinds, plants, upholstered furniture, cluster -Use plastic encasings for mattresses, boxsprings, pillow -There are some products to kill HDM
Describe the clinical presentation of erythema multiforme.: -Erythematous macules and papules that spread -Urticarial plaques that last for many days -Vescilces/bullae -Any combo of these
Describe the clinical presentation of Toxic Epidermal Necrolysis.: -Vesicles/bullae -Necrosis -Systemically ill -Entire epidermis of the lesion can be necrotic and slough off
What are the usual causes of Toxic Epidermal Necrolysis.: -Drugs*** -Toxins -Infections -Neoplasms
What are the usual causes of Erythema Multiforme.: -Drug allergies *** -Trimethoprim/sulfa -Cephalexin
What are some etiologies for feline miliary dermatitis?: -Ectoparasites -Dermatophytes -Allergies -Nutritional -Bacterial -Contact -Autoimmune -Idiopathic
What is a diagnostic plnn for feline miliary dermatitis?: -Examine for parasites -Woods light -DTM culture
What is the clinical presentation of an indolent ulcer?: -Ulcers on upper lip or orally -Female cats (5-6 yrs. Age) -No eosinophils
What is the clinical presentation of an eosinophilic plaque?: -Well circumscribed, raised, ulcerative plaque -Abdomen, back, legs, head, neck -Female cats (3yrs) -Eosinophilic and mast cell infiltration
What is the clinical presentation of a linear granuloma?: -Linear tract on posterior aspect of hind limbs -Severe cases can be seen in the oral cavity -Either sex (1-5yrs) -+/- Eosinophils
How would you identify an indolent ulcer?: -Histopath -Hyperplastic ulcerative dermatitis w/ PMN, plasma cells, mononuclear cell infiltrate -DDX -Squamos cell carcinoma and Fibrosarcoma
How would you identify an eosinophilic plaque?: -Histopath -Eosinophilic and Mast cell infiltrate -Workup -Biopsy -Flea control*** -Hypoallergenic diet -IDST
How would you identify a linear granuloma?: -Histopath -Necrobiosis of collagen w/ histiocytic and multinuclear giant cell infiltrate +/- eosinophils
How would you treat an indolent ulcer?: -Identify and treat underlying cause -Antibiotic trial -Clavamox or Tribissen -Systemic Corticosteriods -Pred -Depo-Medrol REFRACTORY OR RECURRENT: -CO2 laser -Radiation treatment -Cyrosurgery -Immuno-stimulants (Levamisole or Thiabendazole)
How would you treat an eosinophilic plaque?: -Identify and treat underlying cause -Elizabethan collar -Antibiotics -Corticosteriods
How would you treat a linear granuloma?: -Observation -Identify and treat underlying cause -Antibiotics -Corticosteriods -Immuno-stimulants
Describe the clinical presentation of feline plasma cell pododermatitis.: -Non-painful swelling of footpads that may ulcerate Clinical Pathology: -Hypergammaglobuinemia -Lymphocytosis -Neutrophillia
List the potential side effects of progesterone therapy.: -Hyperglycemia (leading to DM) -Acromegaly -Mammary hyperplasia (leading to neoplasia) -Pyometra -Infertility -Behavioral changes
What is cyclosporine? What is its MOA in the treatment of atopy?: -Cyclosporine is an immuno-suppressive drug. MOA: -Suppresses T helper cells -Decreases IgE production -Decreases production of cytokines -Overall decreases skin inflammation and itching
How is canine atopic dermatitis diagnosed?: -Must have at least 3 of the Major Criteria: -Pruritis -Typical morphology and distribution -Involves face, feet, legs -Seasonal or chronic dermatitis -Family or breed predisposition -Must have at least 3 of the Minor Criteria: -Onset of symptoms <3 years of age -Facial erythema and chelilitis (inflammation around lips) -Bilateral conjunctivitis -Superficial staph pyoderma -Increased antigen specific-IgE -Increased antigen-specific IgG4 -Immediate skin test reactivity
Is it possible to cure an atopic dog?: -No, just medically manage dog -However, those animals treated w/ hyposensitization 25% may develop complete remission
What are the major causes of treatment failures in canine atopic dermatitis?: -Client compliance -Donâ€™t remove all possible environmental contaminants -Donâ€™t dose animals medâ€™s correctly
What is the â€œflare factorâ€ relating to atopy?: -The reaction that occurs in response to certain allergen -Fleas are a big flare factor
Why is it important for owners to understand the concepts of summation of effects and pruritic threshold.: Summation of effects: -It is the culmination of all things that can lead to the animals atopy problem -If the owner can understand that there are a whole host of things that play a role in their animals atopy then maybe then can understand why treatment is so difficult and why they must play an active role in the process. Pruritic Threshold: -The level above which the animal will experience atopy -Many factors contribute the animal exceeding the threshold -For example: If fleas are the underlying cause and they are never treated, then the animal can never drop below the pruritic threshold
What are the causes and pathogenesis of food allergies?: Causes: -Sudden reaction to a food source (usually one protein) that triggers an immunological response -a lot are not IgE mediated Patho: -Food allergies can be either a Type I, III, IV hypersensitivity reaction
What is the best way to diagnose a food allergy: -The best way to diagnose food allergy is to do a restrictive diet trial -Symptoms should subside off food (w/in at least 7 days) -Challenges should be reproducible (onset, duration, clinical features) -Symptoms should be gone after each withdrawal
What is an allergen? Antigen?: Allergen: an antigen that stimulates an IgE response (ex. Pollens, dust, animal dander, feathers) Antigen: a substance that elicits an antibody response
How does contact hypersensitivity manifest in animals?: -Lesions usually occur in non-haired areas (feet, ears, ventrum, scrotum, chin, neck) -Pruritis may be the only sign -Severe cases: erythema, vesicles, ulcers, crusts, self-trauma
What are the differences between atopy and contact dermatitis?: Atopy: -A familial predisposition to the development of IgE antibodies and clinical allergy to environmental allergens. Contact dermatitis: -Can either be allergic or irritant Allergic Contact dermatitis: -An inflammatory skin disease caused by a delayed (cell-mediated) response to an antigen or hepten. Requires repeated or continuous exposure to the substance Irritant Contact Dermatitis: -An inflammatory skin disease which occurs within minutes of contact w/ irritating substance
What are the common causes of contact hypersensitivity in dogs?: -Plant or plant pollen -Molds -Meds (neomycin, tetracain, shampoos, insecticides) -Floor wax -Polish or cleaners -Dyes in rugs -Carpets, blankets -Rubber and plastic products
Will anti-histamine creams lessen inflammation in animals w/ contact hypersensitivity? What other treatments would you recommend?: -No anti-histamine are good are prevention, not a treatment once the animal is inflamed Other treatments: -Remove offending agent -Bath after exposure -Topical drying agents (Domeboro) -Topical or systemic corticosteroids -Pentoxiphylline -Topical tacrolimus
What is miliary dermatitis?: -Variable pruritic papulocrustous eruption occurring over dorsum, head, and neck -Millet seed lesions = hemorrhagic crusts
What approach would you follow in treating a cat w/ miliary dermatitis?: 1. Flea control (if they respond, may be the only treatment) 2. Hypoallergenic diets 3. Skin biopsy -Allergic = IDST -Bacterial = C/S and TX -Fungal = DTM and TX -Pemphigus = DFA, TX -Non-specific = Pred -No response = Short term megesterol acetate
What is erythema multiforme?: it is an allergy, usually drug associated
How do you diagnose erythema multiforme?: -Physical Exam -Clinical signs
How do you treat erythema multiforme?: -Removal of drug -Possible corticosteroids??
What is toxic epidermal necrolysis?: full thickness coagulation necrosis of epidermis
How do you diagnose toxic epidermal necrolysis?: -Histopath -full thickness coagulation necrosis of epidermis
How do you treat toxic epidermal necrolysis?: -Correct underlying cause -Supportive care -Pred (be careful there can be a high risk of sepsis)
What is the mechanism involved with a Type II hypersensitivity reaction?: IgG, IgM , Complement + target cell = Lysis and phagocytosis of cell
What is the mechanism involved with a Type III hypersensitivity reaction?: IgG, IgM , Complement + Ag => complexes trapped and attract PMNâ€™s
What is the mechanism involved with a Type IV hypersensitivity reaction?: Cytotoxic action of activated lymphs
What is the mechanism involved with a Type V hypersensitivity reaction?: Ab stimulates cellular response
What are some examples of Type II hypersensitivity reactions?: -BP -SLE -DLE -Drug
What are some examples of Type III hypersensitivity reactions?: -SLE -DLE -Drug -Vasculitis
What are some examples of Type IV hypersensitivity reactions?: -Uveodermatologic Syndrome -SLE -Drugs
What is the pathology of Pemphigus foliaceus?: Pemphigus Ab => binding to pemphigus antigent (desmosome) on keratinocyte => internalization of pemphigus Ab =>activation and release of prteolytic enzymes (plasminogen activator) =>plasminogen converted into plasmin =>plasmin hydrolyzes cell adhesion molecules (desmosomes) =>Acantholysis (blister)
What is the pathology of Pemphigus erythematosus?: Pemphigus Ab => binding to pemphigus antigent (desmosome) on keratinocyte => internalization of pemphigus Ab =>activation and release of prteolytic enzymes (plasminogen activator) =>plasminogen converted into plasmin =>plasmin hydrolyzes cell adhesion molecules (desmosomes) =>Acantholysis (blister)
What is the pathology of Pemphigus vulgaris?: Pemphigus Ab => binding to pemphigus antigent (desmosome) on keratinocyte => internalization of pemphigus Ab =>activation and release of prteolytic enzymes (plasminogen activator) =>plasminogen converted into plasmin =>plasmin hydrolyzes cell adhesion molecules (desmosomes) =>Acantholysis (blister)
What are the lesions associated with pemphigus folliaceus?: Primary = transient pustule =>crust Secondary = -Alopecia -Scale -Erythema -Erosions -Nasal depigmentation -Hyperkeratosis of pads -+/- Pruritis -Face and ear lesions -Oral lesions are RARE +/- Fever and anorexia CAT: -Crusting around nails -Crusting-Alopecia -Scale -Erythema -Erosions -Nasal depigmentation -Hyperkeratosis of pads -+/- Pruritis -Face and ear lesions -Oral lesions are RARE +/- Fever and anorexia CAT: -Crusting around nails -Crusting around nipples around nipples
What are the lesions associated with Pemphigus erythematosus?: Primary lesions: -Pustules to oozing crusts that ocsur on the face (ears, nasal region) -Lesions can also be seen on the paws and genital regions -Erythema -Alopecia -Erosions -Nasal depigmentation -Hyperkeratosis
What are the lesions associated with Pemphigus vulgaris?: -Vesiculobullous => erosive to ulcerative skin lesions +/- pruritis -Oral and MC lesions are common -Can also be seen in axillae, groin, clawbed, paw pad, concave pinna -Fever -Anorexia -Depression -Lymphadenopathy -Pain
What is the histopathology associated with pemphigus folliaceus?: -Acantholytic cells w/ PMN +/-bacteria -Subcorneal pustules w/ acantholytic cells +/- eosinophils
What is the histopathology associated with Pemphigus erythematosus?: -ANA may be positive -Acantholytic cells may be present -Subcorneal pustule +/- cellular infiltrate along the D-E junction
What is the histopathology associated with Pemphigus vulgaris?: -Suprabasilar acantholysis resulting in vesicle/cleft -Basal cells appear as a row of tombstones -+/- dermal infiltrates
What is the pathogenesis of Bullous pemphigoid?: Autoantibodies directed against self-antigens (hemidesmosomes) resulting in blistering just below the epidermis
What is the clinical presentation of Bullous pemphigoid?: -Clinically resemble Pemphigus vulgaris (PV) +/- photoaggrevation -Vesiculobullous (tense) => erosive to ulcerative skin lesions +/- pruritis -Oral MC lesions are common (no oral lesions in pigs) -Axillea, groin, clawbed, paw pad, concave pinna, face -Fever -Anorexia -Depression -Lymphadenopathy -Pain
What is the histopathology associated with Bullous pemphigoid?: -Subepidermal clefting + eosinophils in dog -No acantholysis
What is the pathogenesis of SLE?: 1.Type II hypersensitivity: -Antibodies directed against self-nuclear antigens (DNA, RNA, histones) 2.Type III hypersensitivity: -Antigen-antibody complexes lodged into vascular epithelium, synovium, muscle, skin BMZ 3.Type IV hypersensitivity: -Cell-mediated activity against self-antigen
What are some major signs of SLE?: Skin lesions Polyarthritis Hemolytic anemia Glomerulonephritis Polymyositis Leukopenia Thrombocytopenia
What are some minor signs of SLE?: Fever of unknown origin CNS signs Oral ulceration Lymphadenopathy Pericarditis Pleuritis
What is needed to make a definitive diagnosis of SLE?: 2 Major and serology + -OR- major/2minor and serology +
What is needed to make a probable diagnosis of SLE?: 1 major and serology + -OR- 2 major and serology (-)
What are some triggers of SLE: -Genetics (loss of tolerance) -UV light -Hormones -Infectious agents -Drugs -Chemical exposure
What are some things found in Serology of a patient with SLE?: ANA (high sensitivity) Ab to nuclear material LE (high specificity) ID opsonized nuclear material in PMN and macrophages
What are some differentials for nasal depigmentation?: -Vitilligo (will not loose the normal cobblestone appearance of nose) -Nasal depigmenation (snow nose and Dudley nose) -Nasal solar dermatitis -Contact dermatitis -Uveodermatologic syndrome -PF, PE, PV, BP, DLE, SLE -Drug reaction -Neoplasia
What are some differentials for oral lesions?: -DLE, SLE, PV, BP -Erythema multiforme -Vasculitis -Drug reaction -Neoplasia -Candidiasis -Eosinophillic granuloma -Eosinophillic plaque -Indolent ulcer -Plasma cell stomatitis -Gingival hypertrophy -Erosions (chemical, viral, renal) -Vegatative glossitis
What class of drug is azathioprine (Immuran)?: Anti-metabolite
What class of drug is Chlorambucil (Leukeran)?: Alkylating agent
What immunosuppressive drug should not be used on cats?: Azathioprine (Immuran)
Should Chlorambucil (Leukeran) be used in cats?: Yes, it is the primary choice for use in cats.
What is the MOA of Azathioprine?: Structural analog of natural metabolites that substitute for purines and pyrimidines
What is the MOA of Chlorambucil (Leukeran)?: Cross link DNA
What is the MOA of Cyclophosphamide (Cytoxan)?: Cross link DNA
What is the MOA of Cyclosporine (Sandimmune and Neoral)?: Inhibits Th cells early in the immune response w/ minimal effects on suppressor cells
What are some side affects of Azathioprine?: -Myelosuppression -Hepatopathy -GI effects
What are some side affects of Chlorambucil (Leukeran)?: -Myelsuppression -GI effects
What are some side affects of Cyclophasphamide (Cytoxan)?: -Myelsuppression -GI effects -Sterile hemorrhagic cystitis
What are some side affects of Cyclosporine (Sandimmune and Neoral)?: -Myelsuppression -GI effects -Gingival hyperplasia -Papillomatosis -Nephrotoxicosis -Lymphoma like lesions
What are some side affects of Glucocorticoids?: -PUPD -Polyphagia -GI ulceration -Steroid hepatopahty -Pancreatitis -DM -Muscle weakness -Hypertension (+/- proteinuria) -PTE (dyspnea)
What is the general lesion distribution of pemphigus folliaceus?: -Face, pinna, feet -Perinipple and nails in cats
What is the general lesion distribution of pemphigus erythematosus?: -Nose and face
What is the general lesion distribution of pemphigus vulgaris?: -ORAL -MC -Nailbed -Axillae -Generalized skin
What is the general lesion distribution of Bullous pemphigoid?: -Oral (similar to PV)
What is the general lesion distribution of DLE?: -Nose and face
What is the general lesion distribution of SLE?: -Oral (localized or generalized) -Footpads -Sub Q nodules
Are there systemic effects associated with SLE?: Yes
Are there systemic effects associated with PE?: No
Are there systemic effects associated with DLE?: No
Discuss the lesions of color mutant alopecia including the pathogenesis.: Lesions: -Scaly, dry and brittle hair coat -Papule may be present Patho: -Puppies are usually normal at birth and later the skin becomes diseased -There are defects in the melanization and cortical structures of the affected hair follicles -Melanin clumps in the hair bulbs and shafts and makes it brittle
Describe your therapeutic plan for color mutant alopecia.: -There is no cure, just medical management (do not breed these animals) -Use follicle flushing shampoos (benzoyl peroxide or ethyl lactate) -Antibiotics for secondary infections -Topical emollients and humectants -Thyroid therapy if T4 is low
Describe a diagnostic plan to confirm a diagnosis of dermatomyositis.: -Skin biopsies (looking for liquefaction necrosis of basal cell layers of epidermis, vesicles) -EMG -Muscle biopsies -ANA -Skin scrapings
What are some breeds predisposed to dermatomyositis?: -Collies -Shelties
What are options for treatment for Dermatomyositis?: -Avoid trauma -Pred -Vit. E -Pentoxiphylline -Tetracycline and Niacinamide -Spay and Neuter
Describe the pathogenesis of acral mutilation syndrome.: -It is a sensory neuropathy w/ decreased numbers of spinal ganglia and dorsal roots -Occurs as a slowly progressive postnatal degeneration
Describe the pathogenesis of cutaneous asthenia.: -Cutaneous asthenia (a.k.a. Rubber puppy syndrome) Patho: -Defect in collagen formation -Increased fragility and laxity of skin -In cats the deficiency is of procollagen peptidase
What breeds are predisposed to lethal acrodermatitis?: Bull Terriers
What are some clinical signs of lethal acrodermatitis?: -Growth retardation -Progressive acrodermatitis -Chronic pyoderma -Chronic paronychia -Diarrhea -Pneumonia -Abnormal behavior -Lighter than normal skin pigmentation
What are some diagnostic options for lethal acrodermatitis?: -Breed predisposition -PE findings -Low serum zinc -Low ALKP -Hypercholesterolemia -Decreased lymphocyte blast transformation -Skin biopsy -Parakeratotic hyperkeratosis w/ ulceration and superficial pyoderma
What is the prognosis for LETHAL acrodermatitis?: -Poor -Median survival 7 months -Most puppies die of bronchopeumonias
What are the clinical signs of epidermal dysplasia?: -Lesions begin in puppyhood -Erythema -Pruritis (feet, ventrum at first and then becomes generalized) -Hyperpigmentation -Seborrhea oleosa -Peripheral lymphadenopathys
What breeds are predisposed to epidermal dysplasia?: West highland white terrier
What is the diagnostic plan to diagnose epidermal dysplasia?: -Rule out these diseases (atopy, food allergy, sarcoptes, demodex, ichthyosis, endcrinopathies, other seborrheic diseases) -Skin biopsy: epidermal dysplaisa w/ hyperchromasia -Increased mitosis, crowding of basal keratinocytes w/ â€œ budsâ€, parakeratosis
What is the treatment for Sebaceous adenitis?: -No cure -Life long management 1. Keratolytic shampoo (Sialycylic acid) 2.Tetracycline +/- Niacinamide 3.Vit. A 4.Retinoids ($$$) 5.Cyclosporine
What is the predisposition for Sebaceous adenitis?: -Vizslas -Akita -Samoyed -Standard poodle (black and apricot)
What is the prognosis for Sebaceous adenitis?: -Fair -Trying to minimize symptoms and manage the disease (there is no cure)
How do you diagnose Sebaceous adenitis?: -Histopath: -Granulomatous sebaceous adentitis -Chronic cases have complete absence of sebaceous glands
What is the treatment for ichthyosis?: -Life long (no cure) -Hydrotherapy -Topical antiseborrheias/keratolytic agants -Emollients -Propylene glycol -Retinoids -Vit. A
How do you diagnose Ichthyosis?: -Rule out other causes of seborrhea -Skin biopsy: -Prominent granular layer -Numerous mitotic figures in keratinocytes -Orthokeratotic hyperkeratosis -Follicular keratosis -Plugging
Which breed of cats is predisposed to primary seborrhea oleosa?: Persians
What is follicular dysplasia?: Schnauzer Comedone Syndrom is associated with this.
What is pattern baldness?: ??
What is Ehlers-Danlos syndrome?: -It is cutaneous asthenia (a.k.a.Rubber puppy syndrome) -The skin hangs in loose folds
What is the normal skin extensibility index for dogs and cats?: Extensibilty index = (vertical height of skin fold)/(body length) * 100 -Normal 9-16% and Affected is 18-24 %
What is epidermolysis bullosa?: -Blisters and ulcerations at areas of trauma (footpad, mouth, anus, elbows)
How do you diagnose epidermolysis bullosa?: -Histopath: shows dermoepidermal vesicles and bullae -Electron microscopy
What are the clinical signs of â€œSchnauzer Comedone Syndromeâ€?: -Multiple comedones on the back that become a crusted papule
What is the differential diagnoses need to be ruled out to confirm a diagnosis of Schnauzer Comedone Syndrome?: -Demodex -Dermatophytes -Staph pyoderma -Cushings
Papule: Small solid elevation of skin
Plaque: Solid elevation of skin with a flattened top (> 1 cm)
Macule: Well circumscribed, flat spot characterized by a change in the color of the skin
Patch: A change in skin color > 1-2 cm
Nodule: A circumscribed solid elevation that usually extends into the deeper layers of the skin
Tumor: Soft or firm, movable or fixed masses of various sizes and shapes
Wheal: Sharply circumscribed raised lesion consisting of EDEMA
Pustule: Small circumscribed elevation of the skin containing PUS
Vesicle (bulla): Sharply circumscribed elevation of the skin filled with SERUM OR BLOOD
Scale: Accumulation of loose fragments of the horny layer of the skin
Epidermal Collarette: Peeling edge of epithelium surrounding an erosion or ulcer
Crust: Dried exudates on the surface of a lesion
Furunculosis: Draining tract (sinus) communicating from an area of suppuration to a body surface, usually indicative of ruptured hair follicles and secondary bacterial infections.
Abscess: Accumulation of inflammatory cells and necrotic debris
Hyperpigmentation: Increase in skin pigment (melanosis)
Excoriation: Superficial (epidermal) abrasion caused by self-trauma
Fissure: Linear cleavage into or through the epidermis caused by disease or injury
Ulcer: Break in the epidermis with exposure of the dermis
Scar: Area of fibrous tissue that has replaced the damaged dermis or SQ tissue
Lichenification: Thickening or hardening of the skin with exaggerations of skin markings
Hyperkeratosis: Increased thickness of the horny layers of the skin
Necrosis: An area of dead cells
Comedones: Dilated hair follicles filled with keratin and sebaceous debris
In regards to flea control, what is the MOA of cholinesterase inhibitors?: -Inhibit cholinesterase -It is an organophosphate -Potent w/ good residual effects -Carbamates are safer than organophosphates -Toxic to Cats
In regards to flea control, what is the MOA of Pyrethrins?: -Oil extract from Chrysanthemum flower -Causes extended membrane depolarization -Inactivated by UV light -Rapidly kill -Low residual effect -Piperonyl butoxide often added -Must be re-applied if animal goes outside
In regards to flea control, what is the MOA of Permethrins?: -Synthetic pyrethrin -More UV stable -Fast kill **TOXIC TO CATS** -Found in most OTC flea products
In regards to flea control, what is the MOA of IGRâ€™s?: -Juvenile hormone analogs -Ovicida -Larvicidal -Long residual effect
In regards to flea control, what is the MOA of Lefenuron (Program)?: -Insect development inhibitor -Inhibits chitin synthesis -Stored in body fat -NOT an adulticide (limits its use in FAD) -All contact animals need to be treated -Slow acting -Oral or injectable
In regards to flea control, what is the MOA of Fipronyl (Frontline)?: -Phenylpyrazole -GABA receptor antagonist -Affinity for SQ secretions -Effective against ticks FRONTLINE PLUS: -Fipronyl + Methoprene -Addition of juvenile growth hormone analogs -Prevents emergence of fipronyl resistant flea populations -Can bath animal w/out loosing efficacy -Apply monthly for FAD patients
In regards to flea control, what is the MOA of Imidacloprid (Advantage)?: -Chloronicotinyl compound -Binds to post-synaptic nicotinic receptors -NOT effective against ticks -Efficacy may be decreased by bathing -Apply once a month
In regards to flea control, what is the range of action of Selemectin (Revolution)?: -Activity against fleas, ticks (only Dermacantor variabilis), dirofilaria, sarcoptes, odectes, hooks, and rounds
In regards to flea control, what is the MOA of Citrus Oil?: -Disrupts flea ectoskeleton -Found in many OTC shampooâ€™s -Skin irritation and adverse side effects
In regards to flea control, what is the MOA of Nitenpyram (Capstar)?: -Rapid acting adulticide
In regards to flea control, what is the MOA of Advantix?: -Imidacloprdi + Permethrin -Added efficacy against ticks -Use only in dog households -DO NOT USE ON CATS (toxic even if cat rubs on dog)
What is the basic life-cycle of a flea?: Egg L1 L2 L3 Pupae Adult
What are some characteristics of flea eggs?: -White -Non-sticky -Laid on host and fall into environment to complete life cycle -Hatch in 1-10 days -.5mm in length
What are some characteristics of flea larvae?: -Legless, move by a single row of bristles on each segment -Yellow to white in color -Non-parasitic -Geotactic and photophobic so they move deeper into carpets, cracks in wood, soil -Can move over 40cm in carpet -Feed on organic debris and dried blood -3 molts in larval stage -5-11 days is the larval stage if sufficient food and right climate (dryness, extreme heat or cold are detrimental)
What are some characteristics of flea pupae?: -Sticky cocoon -Highly resistant to desiccation and parasiticides -Peak emergence is 8-9 days -Emergence depends upon: -Temperature -Physical pressure
What are some characteristics of adult flea?: -Small, brown, wingless -Laterally compressed bodies -Attracted to host by: -Movement -Warmth -Carbon dioxide -Live entire life on host (can live on host for up to 100 days) -Female lays eggs 3-4 days after a blood meal -Female can lay 13-35 eggs per day
How would you diagnose a flea allergy?: -History -PE -Intradermal skin tests -Serologic tests -Histopathology -Response to therapy
How would you treat a flea allergy?: -Flea control -Anti-pruritics -Antibiotics if necessary -Immunotherapy if ineffective
What are some clinical signs of a flea allergy in a dog?: -Caudal 1/3 of body -Pruritis -Papules, crusts -Pyotraumatic dermatitis -W/ chronicity can see: -Alopecia -Lichenfication -Hyperpigmentation
What are some clinical signs of a flea allergy in a cat?: -Caudal 1/3 of body and neck -Miliary dermatitis -Symmetric alopecia w/ no lesions -Eosinophilic granuloma complex
Which flea products are toxic to cats?: -Permethrines, Cholinesterase inhibitors
What is the most common species of flea found on the dog? Cat?: -Ctenocephalides felis -Prevelance is greater than 92% in dogs and 97% in cats
How does intermittent vs. continuous exposure to fleas affect a petâ€™s reaction to them?: Intermittent exposure = predisposes animals to FAD (flea atopic dermatitis) Continuous exposure = may lead to tolerance
What the are signs associated w/ pruritus in cats?: -Indolent ulcers (lips) -Granulomatous red lesions on ventrum
What dermatophytes are pathogenic in dogs and cats?: -Microsporum canis (most common) -M. gypseum -Trichophyton mentagrophytes (seen in rodents) -Sporotrichosis?
How are Dermatophytes transmitted?: Dermatophytes are transmitted by contact w/ infected hairs, scales, or fungal elements
What are typical lesions and distribution patterns of dermatophyte infections in dogs?: -Classic lesions: annular areas of peripherally expanding alopecia, scale, crust, papules and pustules -Nasal folliculitis and furunculosis -Generalized seborrhea-like infection -Dermatophytic kerion -Onychomycosis (nail infection) M. Canis Head and front limbs M. gypseum Extremities and tail T. mentagrophytes Whole body
What are typical lesions and distribution patterns of dermatophyte infections in cats?: -Generalized infections are more common: -Alopecia -Folliculitis, erythema, scale, crust, papule -Generalized seborrhea like eruption -Milliary dermatitis = uncommon to be caused by dermatophytes (usually caused by fleas) -Localized infections: -One or more annular areas of alopecia -May mimic chin acne or â€œstud tailâ€ -Onychomycosis -Dermatophyte kerion -Dermatophyte pseudomycetoma
How can you positively identify a fungal agent (genus and species)?: -Most reliable test fore identification = Fungal culture -Identify the organism through morphologic and microscopic characteristics -DTM (dermatophyte test medium) -Dermatophytes utilized the protein in the media first, leading to alkaline metabolites that cause the media to turn red w/in 10-14 days -Saprophytes utilized carbohydrate first creating acidic metabolites
Why is it important to make a definitive diagnosis for a dermatophyte infection?: is important to make a definitive diagnosis in order to properly clear up the problem and prevent re-infection
What recommendations would you make for a cattery w/ dermatomycosis in each litter of kittens (M canis)?: -Cessation of breeding program -Identification and isolation of positive animals -Topical and systemic therapy for positive animals -Topical therapy for contact cats -Strict environmental control -Treat all cats until cats are culture negative 3 times -Toothbrush cultures to screen healthy appearing cats for carrier status
What skin layer do dermatophytes grow in?: -Keratogenous zone of keratinized tissue (Adamsonâ€™s fringe) -Hair, nail, stratum corneum of skin -Donâ€™t affect the hair bulb
Describe the lesions seen with Cryptococcus.: -Cutaneous lesions including nodules, ulcers and draining tracts -Nasal discharge and sneezing -Ocular involvement = blindness -Neural involvement = seizures, ataxia, paresis
What are the risk factors associated with cryptococcus?: More common in cats Found in pigeon shit
How is cryptococcus diagnosed?: -Cytology -Biopsy -Serology
What are the treatment options for Cryptococcus?: -Itraconazole -Fluconazole -Flyctosine
What are the clinical signs of Malassezia dermatitis in a dog?: -Very pruritic GENERALIZED: -Erythematous, greasy, scaly, crusty, malodorous, lichenification, alopecia, hyperpigmentation LOCALIZED: -Otitis, lips, muzzle, interdigital spaces, ventral neck, medial thigh, groin, axilla, paronychia, intertriginous regions -40% have concurrent bacterial pyoderma
What are the clinical signs of Malassezia dermatitis in a cat?: -Not as common as dog GENERALIZED: -Erythematous, scaly to waxy dermatitis LOCALIZED: -Otitis, chin acne, paronychia (base of nail)
How do you diagnose Malassezia?: -Cytologic exam: -Impression smear, swab, skin scraping, acetate prep -Look for round to oval budding yeast â€œpeanut shapedâ€ -Skin biopsy w/ histopath -Culture -Look for a response to anti-yeast therapy
Discuss Treatment for Malassezia.: -Identify and address the underlying cause: -w/ out correction of the predisposing disease or factors, the disease is likely to reoccur -Treat concurrent Staph pyoderma Topical therapy: -Anti-fungal creams or lotions for localized areas -Anti-fungal shampoos for generalized areas -Dips are not necessary but can be effective Systemic therapy: -Ketoconazole or Itraconazole -**Griseofulvin is NOT effective** -Treat 7-14 days past clinical cure
What are the predisposing factors for Malassezia?: -Increased humidity -Immune dysfunction -Genetic (Bassetâ€™s or WHWT) -Hypersensitivity -Keratinization disorders -Endocrine or metabolic disorders
Which of the following are zoonotic? Blastomycosis, Histoplasmosis, Coccidiomycosis, Crytococcus neoformans.: Cryptococcus neoformans
What are some clinical signs associated with Blastomycosis?: -Nodular skin lesions -Draining tracts -Absscesses -Often have concurrent respiratory disease
What are some clinical signs associated with Histoplasmosis?: -GIT and respiratory disease -Granuloma and draining tract skin lesions
What are some clinical signs of Coccidomycosis?: Dog: -Young, male dogs -Coughing, dyspnea, fever, anorexia, wgt. Loss, lameness, ocular disesase -Papules, nodules, abscesses, draining tract, ulcers -Skin infections often occur over infected bone Cat: -RARE -Anorexia, wgt. Loss, cough, dyspnea, lameness, ocular disease, skin lesions
What are some clinical signs of Cryptococcus neoformans infection?: -Cutaneous lesions include nodules, ulcers, draining tracts -Nasal discharge -Ocular involvement = blindness -Neural involvement = seizures, ataxia, paresis
What are some physical characteristics of Blasto?: -Broad based budding -Endemic in Mississippi and Ohio river valley -Ingested or inhaled from: soil, bird or bat shit
What are some physical characteristics of Histo?: -Tiny organism -Endemic in Eastern US
What are some physical characteristics of Coccidio?: -Largest organism w/ spherules that contain endospores -Found in sandy, alkaline soil, high temperature, low rainfall, low elevation -Endemic in SW US, South and Central America
What are some physical characteristics of Cryptococcus neoformans?: -Large organism -Relatively common in cats -Found in pigeon shit -Thick candy shell
Which breed of dog is predisposed to developing cutaneous infections w/ pythium?: GSD
What is the usual source of pythium infection?: Swamps or ponds in southern US
How is pythium treated?: Aggressive surgery (amputation) -Itraconazole + Terbenafine -Treat for 2 months and recheck titers at LSU
What is the prognosis for pythium?: Poor (â€œswamp cancerâ€ is invasive and often fatal)
What is an asymptomatic carrier?: animal that is carrying and possibly shedding a disease without showing any clinical signs
How are asymptomatic carriers identified?: Screening tests
How are Malassezia infections transmitted?: Malassezia is part of the normal flora of ears and skin. It is an opportunistic pathogen that proliferates under conditions of increased moisture (i.e. greasy, scaly, inflamed skin)
Does antibiotic therapy predispose animals to yeast or fungal infections of skin?: Yes
What is the most common subcutaneous fungal infection of cats and dogs?: Microsporum canis
What are the risk factors for infection with Blasto?: -Found in the Mississippi and Ohio River valley -Found in nitrogen rich soil and bat and bird shit
Name some fat sources rich in essential fatty acids.: -Sunflower oil -Corn oil -Soybean oil
What are the differences between omega 6 and omega 3 fatty acids?: OMEGA 6 FA -Predominant in terrestrial plants and animals INCLUDES: -Linoleic acid = maintenance of barrier functions of skin -Gamma-linoleic acid = metabolized into anti-inflammatory PGâ€™s -Arachidonic acid = substrate for inflammatory LTâ€™s and PGâ€™s OMEGA 3 FA -Predominates in marine plants and animals INCLUDES: -Alpha-linoleic acid = it is an eicosapentaneoic acid (EPA) and is metabolized by lipooxygenase and cyclooxygenase to LTâ€™s and PGâ€™s
Explain why omega 3 fatty acids may be beneficial in decreasing inflammation?: -EPA metabolized lipooxygenase and cyclooxygenase to LTâ€™s and PGâ€™s (inflammatory mediators)
Which breed are most commonly affected by vit. A responsive dermatosis?: Cocker Spaniel
What are the usual clinical signs for vit. A responsive dermatosis?: -Thick, inflamed crusty lesions on ventral abdomen and thorax -Frond-like keratinous plugs adhered to their surface
How do you diagnose vit. A responsive dermatosis?: -Histopath -Orthokeratotic hyperkeratosis -Follicular keratosis
What is panniculitis?: inflammation of SQ fat
What is pansteatitis?: inflammation of fat w/ in abdomen
What are the DDX for panniculitis and pansteatitis?: -Bacterial or fungal infection -Autoimmune disease -Physiochemical problem -Hereditary
List 5 diseases which may improve following treatment w/ vit. E.: 1. DLE 2. SLE 3. Epidermolysis bullosa 4. Acanthosis nigricans 5. Demodecosis
What breeds are predisoped to zinc responsive dermatosis?: Syndrome I: -Siberian Huskies, Bull terriers and Alaskan Malamutes (primarily -Has been reported in Doberman Pinschers and Great Danes Syndrome II: -Great Danes, Doberman Pinschers, GSD, German Shorthair pointers, Standard Poodles
What is the characteristic histopathological finding w/ zinc responsive dermatosis?: Marked diffuse and follicular parakeratotic hyperplasia (seen w/ Syndrome II)
What are the causes of Syndrome II zinc responsive dermatosis?: -Over supplementation w/ calcium which causes decreased zinc absorption
What are the characteristic histopathological findings of generic dog food dermatosis?: -Focal epidermal necrosis -Mixed dermal infiltrate -Subacute to chronic dermatitis
Understand the concepts of â€œepidermal turnover timeâ€ and â€œdisorder of keratinizationâ€.: Epidermal Turnover Time:| -Number of days from stratum basale to stratum corneum -22 days in normal dog -3-5 days in dog w/ a disorder of keratinization Disorder of Keratinization: -Alterations in basal cell mitotic rate -Alterations in transformation of cytoplasmic proteins into keratin -Alterations in exfoliation (may result from changes in epidermal lipids)
Outline a diagnostic approach for a dog presenting to your clinic w/ primary complaint of Seborrhea.: Rule Out: -Parasites -Infections -Allergies -Irritants -Metabolic disorders -Nutritional disorders -Biopsy skin
Know the principle of topical therapy as they relate to the symptomatic control of Seborrhea.: -Topical therapy is for its antiseborrheic and keratolytic actions
List indications of use for systemic retinoids and side effects that must be monitored for.: -Diseases of sebaceous glands (first generation) -Keratinization disorders (second generation) -Sebaceous adenitis, Mycosis fungoides, Idiopathic seborrhea (third generation)
Describe the lesions of feline acne including pathogenesis.: Lesions: -Comedones -Papules -Pustules Patho: -Though to be due to improper cleaning of chin -May also be a seborrheic syndrome +/- secondary infection
List three breeds w/ an increased incidence of seasonal flank alopecia.: 1. Airedale terriers 2. English bulldogs 3. Boxers
List four breeds w/ increased incidence of Alopecia X.: 1. Pomerarians 2. Chow Chows 3. Keeshound 4. Samoyed
What treatments would you recommend for acne in a dog?: -Daily cleansing (Benzoyl peroxide, alcohol, antiseptic shampoos, astringent) -Local antibiotics (erythromycin or mupiracin) -+/-Systemic antibiotics -+/-Topical Retin A ointment/lotion
What treatments would you recommend for acne in a cat?: -Observe if non-inflammatory -Clip hair, clean chin (Benzoyl peroxide, alcohol, antiseptic shampoos, astringent) -+/-Local antibiotics and anti-fungals -+/-Systemic antibiotics -+/-Daily cleaning of chin to prevent reoccurence
List 2 Keratolytic agents.: 1. Benzoic Acid 2. Vit. A Keratolytic = promotes softening and dissolution of stratum corneum Keratoplastic = normalized epidermal kinetics and keratinization
List 2 keratoplastic agents.: 1. Coal Tar 2. Salicylic Acid 3. Sulfur
List 2 degreasing agents in medicated shampoos.: 1. Coal Tar 2. Sulfur
Describe the clinical findings that may be suggestive of Sertoli cell tumor.: -Hair loss -Bone marrow suppression -Fatal thrombocytopenia or anemia -Oily seborrhea -Pruritis -Comedones -Linear prepucial hyperpigmentation -Nipple enlargement
List sex hormones produced by the adrenal gland: -Androgens and Estrogens
Describe the lesions distribution pattern typical of seasonal flank alopecia.: -Non-scarring alopecia of thoracolumbar that is bilaterally symmetrical region develops in fall or spring and hair regrows months later
Describe the lesion distribution pattern typical of Alopecia X.: -Bilateral symmetrical alopecia -Dry dull hair coat -Primary hairs lost first -Head and front legs spared
What is the definition of pruritis?: an unpleasant sensation within the skin which evokes the desire to scratch

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Number of cards 250